Increases in vocalization and motor reflex thresholds are influenced by the site of morphine microinjection: Comparisons following administration into the periaqueductal gray, ventral medulla, and spinal subarachnoid space.

Borszcz, George S.

doi:10.1037/0735-7044.109.3.502

Cited by 34 publications

(64 citation statements)

References 84 publications

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“…26–29,35,44 The failure to observe an increase in SMR threshold does not reflect the resistance of this response to antinociceptive treatments. In previous studies, administration of morphine into the rostral ventromedial medulla or ventrolateral periaqueductal gray (vlPAG) produced significant increases in SMR, VDS, and VAD thresholds 8,9,11,14 and the intrathecal administration of morphine, serotonin, or norepinephrine was equally effective in raising SMR, VDS, and VAD thresholds. 15 The capacity of these central treatments to elevate SMR threshold also demonstrates that SMRs are not generated by direct stimulation of the tail musculature.…”

Section: Discussionmentioning

confidence: 93%

NMDA or Non-NMDA Receptor Antagonism Within the Amygdaloid Central Nucleus Suppresses the Affective Dimension of Pain in Rats: Evidence for Hemispheric Synergy

Spuz

Borszcz

2012

The Journal of Pain

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The amygdala contributes to generation of affective behaviors to threats. The prototypical threat to an individual is exposure to a noxious stimulus and the amygdaloid central nucleus (CeA) receives nociceptive input that is mediated by glutamatergic neurotransmission. The present study evaluated the contribution of glutamate receptors in CeA to generation of the affective response to acute pain in rats. Vocalizations that occur following a brief noxious tailshock (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed by bilateral injection into CeA of the NMDA receptor antagonist D-2-amino-5-phosphonovalerate (AP5, 1μg, 2μg, or 4μg) or the non-NMDA receptor antagonist 6-Cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX, .25μg, .5μg, 1μg, or 2μg). Vocalizations that occur during tailshock were suppressed to a lesser degree, whereas, spinal motor reflexes (tail flick and hindlimb movements) were unaffected by injection of AP5 or CNQX into CeA. Unilateral administration of AP5 or CNQX into CeA of either hemisphere also selectively elevated vocalization thresholds. Bilateral administration of AP5 or CNQX produced greater increases in vocalization thresholds than the same doses of antagonists administered unilaterality into either hemisphere indicating synergistic hemispheric interactions. Perspective The amygdala contributes to production of emotional responses to environmental threats. Blocking glutamate neurotransmission within the central nucleus of the amygdala suppressed rats’ emotional response to acute painful stimulation. Understanding the neurobiology underlying emotional responses to pain will provide insights into new treatments for pain and its associated affective disorders.

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Section: Discussionmentioning

confidence: 93%

NMDA or Non-NMDA Receptor Antagonism Within the Amygdaloid Central Nucleus Suppresses the Affective Dimension of Pain in Rats: Evidence for Hemispheric Synergy

Spuz

Borszcz

2012

The Journal of Pain

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“…The utility of this form of tailshock as a noxious stimulus has been extensively discussed(4, 14). The intensity, duration, and timing of tailshocks were controlled by the computer.…”

Section: Methodsmentioning

confidence: 99%

Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

Munn

Harte

Lagman

et al. 2009

The Journal of Pain

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The parafascicular nucleus of the intralaminar thalamus is implicated in the processing of pain affect in both animals and humans. Administration of morphine into nPf results in preferential suppression of the affective reaction to noxious tailshock in rats. The involvement of the ventrolateral periaqueductal gray in mediating the antinociceptive action of morphine injected into nPf was evaluated. Vocalizations that occur after tailshock offset (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed by injection of morphine into nPf. Vocalizations that occur during tailshock were suppressed to a lesser degree, whereas, spinal motor reflexes (tail flick and hindlimb movements) were unaffected by injection of morphine into nPf. Inactivation of the vPAG via the microinjection of muscimol (GABAA agonist) produced dose-dependent antagonism of morphine-induced increases in vocalization thresholds. The results demonstrate that a functional link between the nPf and vPAG in generating the antinociceptive action of morphine injected into nPf. Perspective: Microinjection of morphine into nucleus parafascicular preferentially suppressed rats’ affective reaction to noxious stimulation. This affective analgesia was reversed by inactivation of the ventrolateral periaqueductal gray. Understanding the neurobiology underlying the suppression of pain affect will provide insights into new treatments for pain and its associated affective disorders.

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“…Vocalizations during stimulation are organized in the brainstem (medullary level) whereas vocalization afterdischarges that outlast the actual stimulus are organized in the forebrain, including the amygdala (Borszcz 1995;Borszcz and Leaton 2003;Han and Neugebauer 2005;Nandigama and Borszcz 2003). Ultrasonic vocalizations in the 22-25 kHz range are emitted specifically in response to aversive stimuli and reflect the negative affective state of the animal (Borta et al, 2006;Han et al, 2005a;Han and Neugebauer 2005;Knutson et al, 2002;Ko et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Spinal CGRP1 receptors contribute to supraspinally organized pain behavior and pain-related sensitization of amygdala neurons

Adwanikar¹,

Ji²,

Li³

et al. 2007

Pain

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CGRP receptor activation has been implicated in peripheral and central sensitization. The role of spinal CGRP receptors in supraspinal pain processing and higher integrated pain behavior is not known. Here we studied the effect of spinal inhibition of CGRP1 receptors on supraspinally organized vocalizations and activity of amygdala neurons. Our previous studies showed that pain-related audible and ultrasonic vocalizations are modulated by the central nucleus of the amygdala (CeA).Vocalizations in the audible and ultrasonic range and hindlimb withdrawal thresholds were measured in awake adult rats before and 5-6h after induction of arthritis by intraarticular injections of kaolin and carrageenan into one knee. Extracellular single-unit recordings were made from neurons in the latero-capsular division of the CeA (CeLC) in anesthetized rats before and after arthritis induction. CGRP1 receptor antagonists were applied to the lumbar spinal cord intrathecally (5μl/min) 6h postinduction of arthritis.Spinal administration of peptide (CGRP8-37, 1μM) and non-peptide (BIBN4096BS, 1μM) CGRP1 receptor antagonists significantly inhibited the increased responses of CeLC neurons to mechanical stimulation of the arthritic knee but had no effect under normal conditions. In arthritic rats, the antagonists also inhibited the audible and ultrasonic components of vocalizations evoked by noxious stimuli and increased the threshold of hindlimb withdrawal reflexes. The antagonists had no effect on vocalizations and spinal reflexes in normal rats These data suggest that spinal CGRP1 receptors are not only important for spinal pain mechanisms but also contribute significantly to the transmission of nociceptive information to the amygdala and to higher integrated behavior.

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Increases in vocalization and motor reflex thresholds are influenced by the site of morphine microinjection: Comparisons following administration into the periaqueductal gray, ventral medulla, and spinal subarachnoid space.

Cited by 34 publications

References 84 publications

NMDA or Non-NMDA Receptor Antagonism Within the Amygdaloid Central Nucleus Suppresses the Affective Dimension of Pain in Rats: Evidence for Hemispheric Synergy

NMDA or Non-NMDA Receptor Antagonism Within the Amygdaloid Central Nucleus Suppresses the Affective Dimension of Pain in Rats: Evidence for Hemispheric Synergy

Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

Spinal CGRP1 receptors contribute to supraspinally organized pain behavior and pain-related sensitization of amygdala neurons

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